Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P80404 (GABA transaminase)
 786 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of di-n-propylacetic acid (valproic acid), a gamma-aminobutyric acid transaminase inhibitor, on the luteinizing hormone (LH) and follicle-stimulating hormone (FSH) response to gonadotropin-releasing hormone (LHRH) was studied in five normal women during the proliferative and luteal phases of the menstrual cycle. Valproic acid produced no significant change in the basal serum concentrations of LH, FSH, estradiol, and progesterone in either the proliferative or the luteal phase of the study. In the proliferative phase the delta LH (maximum increment above baseline) following LHRH stimulation rose from 32.8 +/- 21.2 (mean +/- SD) to 52.2 +/- 28.7 mlU/ml (not significant) after valproic acid, while the delta FSH rose from 2.2 +/- 1.1 to 5.0 +/- 3.6 mlU/ml (not significant). Four of the five volunteers showed an augmentation of the delta LH response to LHRH after valproic acid while the fifth subject showed no change. In three subjects the augmented delta LH response after valproic acid was highly significant. By contrast, the delta LH in the luteal phase following LHRH stimulation fell from 65.3 +/- 20.1 to 43.1 +/- 12.9 mlU/ml after valproic acid (p less than 0.03). Corresponding delta FSH values were 2.5 +/- 1.1 and 2.1 +/- 0.8 mlU/ml (not significant). It is speculated that gamma-aminobutyric acid may exert a modulatory role on gonadotropin secretion following LHRH stimulation and that this effect is influenced by the phase of the menstrual cycle.
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PMID:A presumptive role for gamma-aminobutyric acid in the regulation of gonadotropin secretion in man. 681 Jun 97

The involvement of gamma-aminobutyric acid (GABA) in regulation of pituitary gonadotropin-II (GTH-II) release was studied in the goldfish. Intraperitoneal injection of GABA (300 micrograms/g) stimulated an increase in serum GTH-II levels at 30 min postinjection. The GABAA receptor agonist muscimol (0.1-10 micrograms/g) stimulated GTH-II in a dose-dependent manner. Baclofen, a GABAB receptor agonist, had a small but significant stimulatory effect at 1 and 10 micrograms/g; the amount of GTH-II released in response to baclofen was significantly less (P < 0.05) than that released by muscimol. Pretreatment of goldfish with bicuculline, a GABAA receptor antagonist, but not saclofen, a GABAB receptor antagonist, blocked the stimulatory effect of GABA on serum GTH-II. Elevation of brain and pituitary GABA levels with the GABA transaminase inhibitor, gamma-vinyl-GABA (GVG), decreased hypothalamic and pituitary dopamine (DA) turnover rates, indicating that GABA may stimulate GTH-II release in the goldfish by decreasing dopaminergic inhibition of GTH-II release. The release of GTH-II stimulated by muscimol and GVG was potentiated by pharmacological agents that decrease inhibitory dopaminergic tone, indicating that DA may also inhibit GABA-stimulated GTH-II release. Based on the linear 24-h accumulation of GABA in brain and pituitary after GVG injection, implantation of testosterone, estradiol, or progesterone, previously shown to regulate the serum GTH-II release response to gonadotropin-releasing hormone and GABA, was also found to modulate GABA synthesis in the brain and pituitary.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:GABA stimulation of gonadotropin-II release in goldfish: involvement of GABAA receptors, dopamine, and sex steroids. 839 53

Possible involvement of gamma-aminobutyric acid (GABA) in the control of gonadotropin II (GTH II) secretion was investigated during different phases of the seasonal gonadal cycle of the Atlantic croaker (Micropogonias undulatus). Intraperitoneal administration of GABA (100 microgram/g) elicited a significant increase in plasma GTH II levels in croaker with regressed or pre-recrudescence phase gonads, whereas it did not significantly affect GTH II levels during the early- to mid-recrudescence phase of the gonadal cycle in this species. On the other hand, GABA induced a dose-related inhibition of GTH II secretion in fish with fully recrudesced gonads. Similar opposite changes in GTH II levels were observed when croaker with regressed and fully recrudesced gonads were injected with the GABA transaminase inhibitor, gamma-vinyl GABA (10 and 100 microgram/g). This suggests an involvement of endogenous GABA in the control of GTH II secretion. GABA (1-100 microM) did not significantly alter GTH II release from pituitary fragments from regressed or fully recrudesced fish incubated in vitro, suggesting the lack of a major direct influence at the pituitary level. Muscimol (GABAA receptor agonist, 1 microgram/g) treatment mimicked both the stimulatory and inhibitory effects of GABA, whereas injection of baclofen (GABAB receptor agonist, 1 microgram/g) had no significant effect on basal or a gonadotropin-releasing hormone (GnRH) analog-induced GTH II secretion. Pretreatment of fish with bicuculline (1 microgram/g), a GABAA antagonist, completely blocked the stimulatory influence of GABA on GTH II secretion in croaker with regressed gonads and partially blocked the inhibitory effect in individuals with fully recrudesced gonads. The results demonstrate that GABA exerts opposite influences on GTH II secretion at two different stages of the gonadal cycle of croaker, and acts primarily via GABAA type receptors. Thus, GABAergic pathways may be important in mediating seasonal influences on GTH II secretion in this species.
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PMID:GABA exerts stimulatory and inhibitory influences on gonadotropin II secretion in the Atlantic croaker (Micropogonias undulatus). 1020 78